ライフサイエンスコーパス: SVZ

1 SVZ and RMS microglia thus appear to comprise a function

2 SVZ cells also gave rise to proliferative subventricular

3 SVZ-derived neurogenesis after stroke is activity-depend

4 When we ablated SVZ-derived eNPCs during cuprizone-induced demyelination

5 removal of Gli2 or Gli3 does not alter adult SVZ neurogenesis.

6 delivery of Fezf2 in the neonatal and adult SVZ niche, we showed that ectopic Fezf2 expression is su

7 results demonstrate that neonatal and adult SVZ stem cells retain neuronal fate plasticity.

8 The plastic capacity of neonatal and adult SVZ stem/progenitor cells is still largely unknown.

9 ated GLI3(R) is a primary inhibitor of adult SVZ NSC function.

10 identify molecular cues present in the adult SVZ niche during injury, and analyzed their role on NPCs

11 ntial factor in the maintenance of the adult SVZ, and demonstrate that NSCs within the SVZ maintain t

12 tion arrest and differentiation in the adult SVZ.

13 ses Reln in neural stem cells from the adult SVZ.

14 n in nestin-expressing NSCs within the adult SVZ.

15 on associated with a decline of the affected SVZ-stem cell niche in aged mice.

16 30P mice had fewer Mash1+ transit-amplifying SVZ progenitor cells but Snca-/- mice did not.

17 unctional difference between the SC-NPCs and SVZ-NPCs during homeostatic conditions.

18 o the rostral migratory stream, the anterior SVZ, and the dorsal part of the medial and posterior SVZ

19 regulatory role of H3K4me3 within the baboon SVZ, we developed a technique to purify undifferentiated

20 ifferentiated progenitor cells of the baboon SVZ.

21 In the human brain, SVZ cells including local astroglia also express EZH2, c

22 ated levels of H3K4me3 in the MRI-classified SVZ-associated Glioblastoma Multiforme (GBM), which has

23 results reveal an unknown gateway connecting SVZ neurogenesis to neuronal activity-dependent control

24 oarchitecture and neurogenic potential of cV-SVZ.

25 ibe the cytoarchitecture of canine V-SVZ (cV-SVZ), to assess its neurogenic potential, and to compare

26 ltrastructural studies indicated that the cV-SVZ is organized in layers as in humans, but including m

27 alpha-syn loss and human A30P SNCA decrease SVZ proliferation, cell death in the OB and differential

28 ction of Cre recombinase into Pbx2-deficient SVZ stem and progenitor cells carrying floxed alleles of

29 ion, as Ink4a/Arf-deficiency in Ezh2-deleted SVZ NSCs rescues cell proliferation, but neurogenesis re

30 cate that, in toxic models of demyelination, SVZ-derived eNPCs contribute to support axonal survival.

31 (SVZ), the function of ECM in the developing SVZ remains unknown.

32 r cell proliferation (OPC) in the developing SVZ, thereby altering cellular output of the stem cell n

33 and biochemical experiments revealed direct SVZ NSC responses to local acetylcholine release, synerg

34 used to test for the presence of a distinct SVZ and to define the boundaries of the SVZ in developin

35 Tbr2(+) cells are organized into a distinct SVZ in the dorsal ventricular ridge (DVR) of turtle fore

36 Tbr2(+) cells into an anatomically distinct SVZ, both developmentally and evolutionarily, may be sha

37 tomical integration of nonimmortalized donor SVZ-derived murine aNPCs in the dysmyelinated brain at k

38 Cells expressing SVZ markers infiltrated surrounding brain regions.

39 al hyperproliferation of oncogene expressing SVZ cells by facilitating an antiproliferative expressio

40 insult, provides a favorable environment for SVZ-derived oligodendrocyte progenitor generation.

41 roducing cells expressing Dcx migrating from SVZ to the injury sites.

42 ed whether the fate of postnatally generated SVZ neurons can be altered.

43 ith Raclopride in wild-type females improved SVZ cell proliferation, an effect that positively correl

44 i and reduced OB-size without alterations in SVZ neurogenesis.

45 s that underlie aging-associated declines in SVZ neurogenesis for the early detection of differences

46 rease in cell death-levels and a decrease in SVZ-derived neuroblasts in the distal RMS, as compared t

47 inogen inhibited neuronal differentiation in SVZ and hippocampal NSPCs while promoting astrogenesis v

48 rived IGF2 contributes to NSC maintenance in SVZ but not in the SGZ, and that this is regulated by th

49 at revealed a higher neurogenic potential in SVZ-NPCs compared with SC-NPCs.

50 loss of NSCs and a progressive reduction in SVZ proliferation, without an increase in glial cell pro

51 for neurogenesis independent of its role in SVZ NSC proliferation, as Ink4a/Arf-deficiency in Ezh2-d

52 s inactivation caused rostrocaudal shifts in SVZ and CP gene expression, with loss of corticospinal a

53 l growth factor receptor (EGFR) signaling in SVZ NPCs stimulates the interaction between N-cadherin a

54 ed severe defects in cortical-injury-induced SVZ astrogenesis, instead producing cells expressing Dcx

55 imary neurospheres produced from the injured SVZ increased approximately twofold versus controls, and

56 nic mice to fate map and to selectively kill SVZ-derived eNPCs in the cuprizone demyelination model,

57 s of the transcriptome of dorsal and lateral SVZ in early postnatal mice, including neural stem cells

58 all molecules that can be used to manipulate SVZ microdomain-specific lineages.

59 First, we fate mapped SVZ-eNPCs in cuprizone-induced demyelination and found t

60 I, the number of Ki67(+) cells in the medial SVZ of the injured hemisphere increased.

61 ches in transgenic SVZ-lineage-tracing mice, SVZ-derived neurons synaptically integrate into the peri

62 ell and OPC proliferation in the adult mouse SVZ following demyelination.

63 neural stem cells (NSCs) of the adult mouse SVZ, but its role there has not been elucidated.

64 Mutant SVZ cells overexpressed Wnt, cell-cycle and stem cell ge

65 Synaptic transmission from these newborn SVZ-derived neurons is critical for spontaneous recovery

66 iate activation of genes associated with non-SVZ neuronal subtypes.

67 mical, proteomic, and functional analyses of SVZ NPC-secreted factors revealed the neurite outgrowth-

68 Proteomic analysis of SVZ tissue from mice with experimental demyelination ide

69 is ratio with KLK3 and RUNX3; association of SVZ involvement with Ras oncogene family members, such a

70 maging, we examined the dynamic behaviors of SVZ progenitors in the ferret, a gyrencephalic carnivore

71 pict microglia as a conspicuous component of SVZ and its anterior extension, the rostral migratory st

72 ortical injury, reducing the contribution of SVZ-derived reactive astrocytes to lesion scar formation

73 Our results show an initial decrease of SVZ proliferation at 24 h, followed by a recovery leadin

74 ession is sufficient to redirect the fate of SVZ stem cells.

75 , were causally related to the impairment of SVZ-NPCs.

76 sult in ventriculomegaly with an increase of SVZ neuroblast in rostral migratory stream, whereas VEGF

77 nstrated that proliferation and migration of SVZ neuroprogenitor cells were enhanced by 9cRA.

78 emyelination model, we observed migration of SVZ-eNPCs after injury and their contribution to oligode

79 opathy correlate with an increased number of SVZ OPCs, suggesting ET-1's role as a regulator of glial

80 The number of SVZ stem cells (BrdU+GFAP+) was decreased in SNCA-A30P m

81 We investigated the evolutionary origin of SVZ neural precursor cells in the prenatal cerebral cort

82 males also had reduced neuronal phenotype of SVZ newborn cells and increased striatal neuronal maturi

83 s are expressed during the normal program of SVZ neurogenesis, suggesting that PBX1 might act as a pr

84 that N-cadherin enhances the recruitment of SVZ NPCs into demyelinated lesions.

85 now show that Pbx1 is an early regulator of SVZ neurogenesis.

86 blocked the deleterious effect of cocaine on SVZ cell proliferation in males.

87 n, the sex-specific D1R and D2R signaling on SVZ cell proliferation, neural progenitor and neuronal m

88 ur study is the first to demonstrate ongoing SVZ astrogliogenesis in the normal adult mammalian foreb

89 Significantly, analysis of the neonatal (P5) SVZ reveals that although progenitors remain sensitive t

90 the dorsal part of the medial and posterior SVZ.

91 the ventral part of the medial and posterior SVZ.

92 restructuring of ECM in the early postnatal SVZ.

93 T-1), a molecular component of the postnatal SVZ, promotes radial glial cell maintenance and prolifer

94 Elevated levels of SOX5/6/21 promoted SVZ cells to exit the cell cycle, whereas genetic ablati

95 tential new therapeutic target for promoting SVZ-mediated cellular repair.

96 d radial unit production together with rapid SVZ growth and heightened localized neurogenesis can cau

97 from discrete circuits can directly regulate SVZ neurogenesis.

98 lasts and disorganized astrocytes in the RMS/SVZ, linking EphA4 forward signaling to SVZ and RMS spat

99 ase (ChAT)(+) neurons residing in the rodent SVZ neurogenic niche.

100 Tsc1(null) newborn neurons although sparing SVZ stem cells.

101 prizone-induced demyelination and found that SVZ endogenous neural stem/precursor cells are recruited

102 However, recent studies have shown that SVZ size and the abundance of resident progenitors do no

103 howed a progressive loss of NSCs both at the SVZ and the DG of the hippocampus.

104 oduction of neuroblasts is controlled by the SVZ microenvironmental niche.

105 ns this propensity of glioma to colonize the SVZ through secretion of chemoattractant signals toward

106 stained AZ and PSD markers; in contrast, the SVZ-AZ spatial coupling is decreased.

107 NPCs were isolated and propagated from the SVZ and cervical, thoracic, and caudal regions of the SC

108 ped astrocytes also flow anteriorly from the SVZ in association with the rostral migratory stream, bu

109 The entry of new astrocytes from the SVZ into the corpus callosum appears to be balanced by a

110 ulator of NSPC-derived astrogenesis from the SVZ niche via BMP receptor signaling pathway following i

111 ural stem cells (NSCs) were derived from the SVZ on postnatal 7 d, 1 m, and 12 m-old mice.

112 lasts that appeared to be recruited from the SVZ to the striatum.

113 of the neuroblast ectopic migration from the SVZ toward the lesion showed an increase in this process

114 versity of neural cells originating from the SVZ.

115 We found that microglia residing in the SVZ and adjacent rostral migratory stream (RMS) comprise

116 , BMP, and activin signaling pathways in the SVZ and DG after injury, suggesting that these pathways

117 neural precursor cell (NPC) turnover in the SVZ but it was not addressed if a reduced demand specifi

118 role of APP in regulating NSC number in the SVZ clearly demonstrate that endothelial deletion of App

119 Expression of the PBC protein PBX1 in the SVZ has been reported, but its functional role(s) has no

120 The "intermediate map" in the SVZ is modulated by Eomes (also known as Tbr2), a T-box

121 IP1 and found that expression of DKK3 in the SVZ is restricted to NPCs.

122 blood-derived fibrinogen is enriched in the SVZ niche following distant cortical brain injury in mic

123 favour astrogenesis over neurogenesis in the SVZ niche, and whether astrocytes produced there have di

124 to other unique populations residing in the SVZ niche, microglia display distinct morphofunctional p

125 Lastly, high levels of ET-1 in the SVZ of patients with Cathepsin A-related arteriopathy wi

126 br2-expressing neural precursor cells in the SVZ produce excitatory neurons for each cortical layer i

127 ediate progenitor cells, which divide in the SVZ to produce cortical neurons.

128 n of proliferating neural progenitors in the SVZ was reduced, whereas the proportion of neuroblasts w

129 decreased proliferation and pool size in the SVZ zone, and were associated with elevated inflammatory

130 e cells (resembling neural stem cells in the SVZ), (2) neuronal cells, and (3) a cell type with an in

131 ophin expression is strongly enriched in the SVZ, and pleiotrophin knock down starkly reduced glioma

132 In the SVZ, paracrine IGF2 is a cerebrospinal fluid and endothe

133 xpression of thrombospondin 4 (Thbs4) in the SVZ, revealing a key transcriptional node regulating rea

134 e number of BrdU label-retaining NSCs in the SVZ, whereas NSC/astrocyte deletion of App has no detect

135 molecules to direct germinal activity in the SVZ, which has therapeutic potential in neurodegenerativ

136 dispersal, restricting glioma growth in the SVZ.

137 ectively, miR17-92 cluster expression in the SVZ.

138 ntermediate progenitors, which divide in the SVZ.

139 on aggravates the effect of Snca loss in the SVZ.

140 NSC growth to control the NSC number in the SVZ.

141 cs of alternatively activated microglia, the SVZ/RMS microglia were clearly distinguished by their lo

142 e in one of the adult neurogenic niches, the SVZ.

143 within the dense astroglial meshwork of the SVZ and rostral migratory stream (RMS), yet are permissi

144 t neonatal H-I alters the composition of the SVZ and that LIF is a key regulator for a subset of inte

145 NG2 chondroitin sulfate proteoglycans of the SVZ extracellular matrix.

146 inct SVZ and to define the boundaries of the SVZ in developing cortices.

147 down starkly reduced glioma invasion of the SVZ in the murine brain.

148 on, leading to enhanced migration out of the SVZ into demyelinated lesions of the SCWM.

149 rating both the assembly and function of the SVZ neural stem cell niche.

150 ed by ADAM10 cleavage is the response of the SVZ niche to promote repair of the injured brain.

151 nance of adult NSCs and stabilization of the SVZ vascular niche using conditional, tamoxifen-inducibl

152 as preceded by significant regression of the SVZ vasculature at 14 d, and concomitant decrease of VEG

153 By applying this to NSC of the SVZ, we highlighted the importance of adult neurogenesis

154 nus neurotoxin silencing specifically of the SVZ-derived neurons disrupts the formation of these syna

155 lps NSCs maintain their stemness outside the SVZ in Nes-CreER(T2); Qk(L/L); Pten(L/L); Trp53(L/L) mic

156 s but fails to maintain stemness outside the SVZ.

157 as are GFAP(+) astrocytes found outside the SVZ.

158 re-GEPCOT cells survived and repopulated the SVZ.

159 In rodents, the SVZ is a lifelong source of new neurons fated to migrate

160 rigin of the dopaminergic innervation to the SVZ and SGZ in rodents.

161 prominent in rostral regions adjacent to the SVZ where NPC-derived oligodendrocytes significantly out

162 as been found to innervate proximally to the SVZ, causes motor and cognitive impairments.

163 midbrain dopaminergic projections toward the SVZ.

164 nogen reduced astrocyte formation within the SVZ after cortical injury, reducing the contribution of

165 a significant loss of YFP(+) NSCs within the SVZ by 45 d post recombination, which was preceded by si

166 lt SVZ, and demonstrate that NSCs within the SVZ maintain the integrity of their vascular niche throu

167 undifferentiated progenitor cells within the SVZ of adult baboon brain.

168 The microenvironment within the SVZ stem cell niche controls NSPC fate.

169 ons of neuroblasts and astrocytes within the SVZ/RMS/OB system resulting in a cell-specific mosaic, s

170 ineage tracing demonstrated that it is these SVZ-generated Thbs4(hi) astrocytes, and not Dcx(+) neuro

171 e found preferentially in close proximity to SVZ neural stem cells (NSCs) that produce interleukin-15

172 RMS/SVZ, linking EphA4 forward signaling to SVZ and RMS spatial organization, orientation, and regul

173 nd ROCK inhibition decreased invasion toward SVZ NPC-secreted factors.

174 plasmid polyplexes can non-virally transfect SVZ NPCs when directly injected in the lateral ventricle

175 ng and rabies virus approaches in transgenic SVZ-lineage-tracing mice, SVZ-derived neurons synaptical

176 loped a technique to purify undifferentiated SVZ cells while preserving the endogenous nature without

177 ration of purified quiescent and activated V-SVZ stem cells and transit-amplifying cells.

178 to describe the cytoarchitecture of canine V-SVZ (cV-SVZ), to assess its neurogenic potential, and to

179 onist or antagonist increased or decreased V-SVZ proliferation, respectively.

180 ulting in loss of adult NSCs and defective V-SVZ regeneration.

181 We highlight how V-SVZ NSCs are regulated by local signals from their immed

182 Understanding how V-SVZ NSCs establish and maintain lifelong neurogenesis co

183 However, V-SVZ NSCs are heterogeneous: they have different embryoni

184 great similarity between canine and human V-SVZ indicating that the dog may be better representative

185 dulating the activity of this hypothalamic-V-SVZ connection.

186 o-determine neuronal output from the mouse V-SVZ in both quantitative and qualitative ways in early p

187 purified vascular cells from a neurogenic (V-SVZ) and non-neurogenic brain region (cortex) on the V-S

188 l specification and cell division modes of V-SVZ NSCs, and draw comparisons with NSCs in the SGZ.

189 apoptosis and neuronal differentiation of V-SVZ progenitors before and after birth, and we identifie

190 cal signals had the most potent effects on V-SVZ proliferation and neurogenesis, highlighting the int

191 ic Hh-regulated subregion of the postnatal V-SVZ.

192 endothelial-derived mitogen that promotes V-SVZ cell proliferation.

193 -3 acts as a mediator of quiescence in the V-SVZ adult neural stem cell niche.

194 e evidence that its normal function in the V-SVZ also involves non-autonomous mechanisms.

195 cond-most common dividing cell type in the V-SVZ and had a T(C) of 18 h and T(S) of 9 h.

196 C cells), and neuroblasts (A cells) in the V-SVZ and the number of times these cells divide remain un

197 osis, suggesting a supportive role for the V-SVZ environment in tumor initiation or progression.

198 vides long-range regionalized input to the V-SVZ niche and can regulate specific NSC subpopulations.

199 aired the differentiation potential of the V-SVZ niche in a cell-autonomous fashion.

200 s regarding the unique organization of the V-SVZ NSC niche, the multiple regulatory controls of neuro

201 on-neurogenic brain region (cortex) on the V-SVZ stem cell lineage in vitro.

202 A largely ignored component of the V-SVZ stem cell niche is the lateral ventricle choroid ple

203 view, we describe unique components of the V-SVZ that may permit or promote tumor growth within the r

204 he expanded NSC pool was maintained in the V-SVZ until old age.

205 l circuitry, via mosaic innervation of the V-SVZ, can recruit distinct NSC pools, allowing on-demand

206 presented perivascular niches outside the V-SVZ.

207 maintain the proper niche capacity of the V-SVZ.

208 selectively innervate the anterior ventral V-SVZ and promote the proliferation of Nkx2.1(+) NSCs and

209 MC) neurons innervate the anterior ventral V-SVZ and regulate deep granule interneuron production dep

210 progenitor domains in the anterior ventral V-SVZ of both the neonatal and adult mouse brain.

211 decreased neurogenesis only in the ventral V-SVZ.

212 st in the ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ), which are specializ

213 ls in the ventricular-subventricular zone (V-SVZ) contact the cerebrospinal fluid (CSF), which flows

214 ult mouse ventricular-subventricular zone (V-SVZ) exhibit a regional identity and, depending on their

215 The ventricular-subventricular zone (V-SVZ) is an extensive germinal niche containing neural st

216 st in the ventricular-subventricular zone (V-SVZ) of the adult mammalian brain.

217 ns of the ventricular-subventricular zone (V-SVZ) of the adult rodent brain generate several subtypes

218 mammalian ventricular-subventricular zone (V-SVZ) presents the highest neurogenic potential in the br

219 s) in the ventricular-subventricular zone (V-SVZ) produce diverse olfactory bulb (OB) neurons.

220 is in the ventricular-subventricular zone (V-SVZ) shortly after birth was also largely unaffected, ex

221 he of the ventricular-subventricular zone (V-SVZ), beyond serving as a potential site of origin, affe

222 postnatal ventricular-subventricular zone (V-SVZ), in which neural stem cells generate olfactory bulb

223 the adult ventricular-subventricular zone (V-SVZ), NSCs are a specialized form of astrocyte that gene

224 In the ventricular-subventricular zone (V-SVZ), quiescent neural stem cells (qNSCs) become activat

225 rain, the ventricular-subventricular zone (V-SVZ), replenish olfactory neurons throughout life.

226 ulate the ventricular-subventricular zone (V-SVZ).

227 the adult ventricular-subventricular zone (V-SVZ).

228 ergo increased apoptosis, indicating that VZ/SVZ-derived and rhombic lip-derived progenitor cells sho

229 of EphB2 disrupted the separation of the VZ/SVZ and IZ migratory routes.

230 promoting tangential migration along the VZ/SVZ but not IZ.

231 In contrast, neural progenitors of the VZ/SVZ did not undergo increased apoptosis, indicating that

232 the ventricular zone/subventricular zone (VZ/SVZ) and intermediate zone (IZ) of the dorsal telencepha

233 ed in NPCs of the mouse subventricular zone (SVZ) and aged animals with genetically enhanced WIP1 exp

234 ult neurogenesis in the subventricular zone (SVZ) and in the subgranular zone (SGZ) of the hippocampu

235 ridine (+) cells in the subventricular zone (SVZ) and lesioned cortex in the stroke brain.

236 protein changes in the subventricular zone (SVZ) and neurodegenerative diseases with age.

237 of the brain, e.g., the subventricular zone (SVZ) and substantia nigra (SN), have promising potential

238 the elaboration of the subventricular zone (SVZ) and the associated increase in neural progenitors.

239 ous neurogenesis in the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampus, wher

240 enesis in the forebrain subventricular zone (SVZ) and the hippocampal dentate gyrus (DG).

241 ammals occurring in the subventricular zone (SVZ) and the subgranular zone (SGZ), is subject to compl

242 in the early postnatal subventricular zone (SVZ) are critical for proper brain development yet remai

243 and progenitor cells of subventricular zone (SVZ) are isolated and expanded using the neurosphere ass

244 s (NPCs) from the adult subventricular zone (SVZ) can also generate new oligodendrocytes after demyel

245 itor cells of the mouse subventricular zone (SVZ) caused several distinct effects: 1) the number of d

246 We challenged subventricular zone (SVZ) cells in vivo with low concentrations of CNTF to an

247 s) originating from the subventricular zone (SVZ) contribute to brain repair during CNS disease.

248 e retained in the brain subventricular zone (SVZ) during the chronic phase of multiple sclerosis in h

249 nces and found that the subventricular zone (SVZ) expanded massively during the early second trimeste

250 last chain formation in subventricular zone (SVZ) explants are compromised when clusterin, which is p

251 SCs) in the adult mouse subventricular zone (SVZ) express the histone methyltransferase EZH2.

252 irth, stem cells in the subventricular zone (SVZ) generate neuroblasts that migrate along the rostral

253 lls (NPCs) found in the subventricular zone (SVZ) have prompted strategies targeting gene therapies t

254 l niche in the affected subventricular zone (SVZ) in aging mice.

255 neurogenesis within the subventricular zone (SVZ) in the rodent model.

256 within the adult neural subventricular zone (SVZ) in vivo, we show distinct responses to ionising rad

257 ality, mass effect, and subventricular zone (SVZ) involvement-were independently evaluated and correl

258 The lateral ventricle subventricular zone (SVZ) is a frequent and consequential site of pediatric a

259 The subventricular zone (SVZ) is greatly expanded in primates with gyrencephalic

260 The subventricular zone (SVZ) is the largest germinal zone of the forebrain and i

261 enerated from nestin(+) subventricular zone (SVZ) neural progenitor cells (NPCs) in normal adult mice

262 neurogenesis from adult subventricular zone (SVZ) neural stem cells (NSCs) in culture.

263 newly generated rodent subventricular zone (SVZ) neuroblasts as they transit along the lateral ventr

264 Subventricular zone (SVZ) neurogenesis continuously provides new GABA- and do

265 in the control of adult subventricular zone (SVZ) neurogenesis in rodents.

266 Postnatal and adult subventricular zone (SVZ) neurogenesis is believed to be primarily controlled

267 factor (BDNF) level and subventricular zone (SVZ) neurogenesis.

268 lls (NPCs) of the adult subventricular zone (SVZ) niche are fairly well understood, the pathways acti

269 (NSC) pool in the adult subventricular zone (SVZ) niche by preventing premature differentiation of NS

270 of these cells in their subventricular zone (SVZ) niches but fails to maintain stemness outside the S

271 mouse lateral ventricle subventricular zone (SVZ) NICs as Glast(mid)EGFR(high)PlexinB2(high)CD24(-/lo

272 genitor cells or in the subventricular zone (SVZ) of ischemic animals significantly increased cell pr

273 ssed Idh1(R132H) in the subventricular zone (SVZ) of the adult mouse brain.

274 ent from the neurogenic subventricular zone (SVZ) of the adult mouse striatum.

275 lar niche signal in the subventricular zone (SVZ) of the lateral ventricle of the adult mouse brain.

276 maturity (NeuN) in the subventricular zone (SVZ) of the lateral ventricles and striatum of mice with

277 esis takes place is the subventricular zone (SVZ) of the lateral ventricles.

278 lation drives increased subventricular zone (SVZ) progenitor proliferation, migration, and neuronal m

279 alling is necessary for subventricular zone (SVZ) proliferation and olfactory bulb (OB) neurogenesis.

280 The subventricular zone (SVZ) provides a constant supply of new neurons to the ol

281 PCs) located within the subventricular zone (SVZ) since this latter area is considered one of the pri

282 The adult subventricular zone (SVZ) stem cell niche is comprised of multi-ciliated epen

283 (eNPCs) located in the subventricular zone (SVZ) to generate new OPCs in the lesion site has been de

284 se in stem cells of the subventricular zone (SVZ) upon oncogenic stress, whereas their expression in

285 stem cells (NSC) of the subventricular zone (SVZ) were temporarily expanded by conditional expression

286 r19 are observed in the subventricular zone (SVZ), but are distantly segregated from multi focal Type

287 lactosidase outside the subventricular zone (SVZ), subarachnoid hemorrhage, and ventriculomegaly.

288 quiescence in the adult subventricular zone (SVZ), the function of ECM in the developing SVZ remains

289 oglial functions in the subventricular zone (SVZ), the major postnatal neurogenic niche.

290 d RhoA and Cdc42 in the subventricular zone (SVZ), where more fate-restricted progenitors are located

291 Subventricular zone (SVZ)-derived adult neural precursor cells (aNPCs) were i

292 ursors (NPs) within the subventricular zone (SVZ).

293 regions, including the subventricular zone (SVZ).

294 ced neurogenesis in the subventricular zone (SVZ).

295 ive astrocytes from the subventricular zone (SVZ).

296 ction also homed in the subventricular zone (SVZ).

297 NPCs derived from the subventricular zone (SVZ-NPCs) were also included in the study as a reference

298 lls located within the Sub-Ventricular Zone (SVZ).

299 t zones, including presynaptic vesicle zone (SVZ), active zone (AZ) and postsynaptic density (PSD).

300 c ventricular (VZ) and subventricular zones (SVZ), which give rise to excitatory neurons, are divided